Abstract
Liver injury—expressed as elevated liver enzymes—is common in patients with COVID-19. Little is known about the potential mechanisms of liver damage by SARS-CoV-2. A direct cytopathic effect on hepatocytes as well as injury related to hypoxia or hepatotoxicity are being considered. The aim of the study was to compare the clinical characteristic of COVID-19 disease in patients with normal and abnormal liver enzymes activity. A group of 150 patients with COVID-19, hospitalized in our center, was analyzed. Patients with the known liver comorbidities were excluded (n = 15). Clinical features and laboratory parameters were compared between patients with normal and abnormal aminotransferase values. Liver injury expressed as any alanine aminotransferase (ALT) elevation was noted in 45.6% of patients hospitalized due to COVID-19. The frequencies of aspartate aminotransferase (AST) elevation were lower. It was noted that elevated ALT/AST unfavorably affected other parameters related to liver function such as albumin level; gamma-glutamyl transpeptidase (GGTP); and partly, ALP activity and influenced inflammation-related parameters. The most probable cause of mild hepatitis during COVID-19 was anoxia and immune-mediated damage due to the inflammatory response following SARS-CoV-2 infection. A direct cytopathic effect of SARS-CoV-2 on hepatocytes, albeit less probable, can be considered as well. The use of potentially hepatotoxic drugs may contribute to liver damage.
Highlights
IntroductionIn late December 2019, China reported a cluster of severe pulmonary infections of unknown cause in Wuhan City, Hubei Province
The aim of our study was to compare clinical characteristic of COVID-19 disease in patients with normal and abnormal liver enzymes activity to evaluate the possible mechanisms of liver injury, especially the relation with oxygen dependence, inflammatory parameters, and drugs used for antiviral treatment
Fifteen patients were excluded from further analyses due to concomitant liver disease, among them, n = 8 (5.3%) had nonalcoholic fatty liver disease (NAFLD), n = 5 (3.3%) had alcoholic liver disease (ALD), n = 1 (0.7%) had acute hepatitis A infection, and n = 1 (0.7%) had liver and kidney dysfunction in the course of systemic lupus
Summary
In late December 2019, China reported a cluster of severe pulmonary infections of unknown cause in Wuhan City, Hubei Province. SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2; previously: novel coronavirus or 2019-nCoV) emerging in humans was confirmed as the cause of this severe acute respiratory syndrome, subsequently named coronavirus disease 2019 (COVID-19, previously: 2019-nCoV acute respiratory disease) [1–5]. Researchers consider horseshoe bats as the most likely natural reservoir for SARS-CoV-2. SARS-CoV-2 has been spreading rapidly throughout the world—on 11 March 2020, the World Health Organization (WHO)
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